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Antiarrhythmic drugs

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Goal: suppress dysrthymia formation. Maintain effective cardiac output by stabilizing cardiac rhythm. General characteristics of antiarrhythmic drugs A. There is no drug found to be completely safe and effective. No universal agent no one drug for all types of arrhythmias B. Used in acute treatment of dysrhythmias. Lose Normal Sinus Rhythm (NSR) Get NSR back. Block the AV node slow impulses to ventricles C. Prodysrhythmic effects Worsen existing dysrhythmias and precipitate new ones. May suppress one type cause or worsen others. Remember that virtually all dysrhythmic drugs have this effect. D. Drugs have come and gone, recommendations/indications for their use have changed E. Current drug therapy is not always contemporary. Many patients are still on older drugs F. Decline in drug use due to success of nonpharmacological techniques (catheter ablation & implantable defibrillators) are more successful in managing certain types of dysrhythmias. G. Most are classified by their effects on the cardiac action potential Classification of antiarrhythmic drugs A. Traditionally antiarrhythmics placed into classes the Singh Vaughn Williams classification 1. Class I - drugs that block Na channels. By blocking Na drugs slow impulse conduction in the atria and ventricles. Further divided into subclasses. Subclasses A, B, C, D a. I-A (examples: quinidine, procainamide, disopyramide) b. I-B (examples: Lidocaine and orally effective lidocaine alternatives c. I-C (examples: propafenone, encainide, flecainide) 2. Class II,sympatholytics- drugs that decrease SA node automaticity, AV conduction velocity, and myocardial contractility ( Beta Blockers) 3. Class III, drugs Block potassium (K) channels. Delay repolarization and prolong the relative refractory period. Prolong repolarization, mainly via blocking outward K channels. (e.g. amiodarone, dofetilide, bretylium) 4. Class IV, drugs that block calcium channels (e.g. Verapamil)

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Drugs Mainly (Nowadays) for Supraventricular Arrhythmias

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Quinidine (Class 1A) an old drug that is still around (18th century, largest class) A. Used mainly for supraventricular (atrial) arrhythmias, e.g. atrial fibrillation 1. Side effect hypotension, GI upset Cinchonism a characteristic syndrome of quinidine toxicity includes GI upset, tinnitus, visual disturbances, and dizziness. 2. Quinidine interferes with digoxin excretion, increases digoxin toxicity Procainamide (Pronestyl) - blocks sodium ion channels in myocardial cells A. Correct many different types of atrial and ventricular dysrhythmias (broad-spectrum drug) 1. Side effects N/V, abdominal pain, headache; may produce new dysrhythmias, or worsen existing ones 2. Lupus-like syndrome Class I-C agents: Flecainide (Tambocor), propafenone (Rythmol) A. Orally effective

2 B. Severe ventricular dysrhythmias, contemporary use Patients with AFIB who do not IV.
have good ejection fraction C. Side effects dizziness, blurred vision Propranolol (Inderal) (Prototype of Class II, Beta blockers) A. Mainly used to treat sinus tachycardia, esp. if caused by excessive sympathetic stimulation B. Affect on autonomic nervous system, BB slow the heart rate and decrease conduction velocity through the AV node. Myocardial automaticity is reduced, & many types of dysrhythmias are stabilized C. Main value of BB as Antidysrhythmic agents is to treat atrial dysrhythmias associated with heart failure. In post MI patients BB decrease likelihood of sudden death owing to their Antidysrhythmic effects D. Side effects Bradycardia, hypotension ( may cause dizziness, syncope); BB that are not cardioselective may affect beta2 adrenergic receptors affect lungs possibly causing bronchospasm E. Sotalol (Betapace, oral) esmolol (Brevibloc; Parenteral) other beta blockers used for arrhythmia management. Amiodarone (Cordarone; Prototype Class III) A. Latest American Heart Assn. ACLS protocols have amiodarone (IV) as first-choice drug (after epinephrine) for various arrhythmias/ conditions including ventricular fibrillation B. Now being used more, earlier, for supraventricular arrhythmias (AFIB) C. Key adverse effect (main concern repeated/long use) 1. common N/V 2. common/serious due to fact 37% of it has iodine remember the 6 Ps a. Pigmentation b. Photosensitivity c. pulmonary fibrosis (life threatening) d. peripheral neuropathy e. Pueking N/V most common SE* f. Prolonged PR interval 3. Interferes with T3 T4 conversion - hypo or hyperthyroidism Calcium channel blockers (CCBs) Verapamil (Isoptin, Calan), diltiazem (Cardizem) A. By slowing conduction velocity, they are able to stabilize certain dysrhythmias B. Effects include reduced automaticity in the SA node and slowed impulse conduction through the AV node. This slows the heart rate and prolongs the refractory period C. CCBs effective only against supraventricular dysrhythmias

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Drugs Mainly for Ventricular Arrhythmias

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Lidocaine (Xylocaine; Class IB) 4:1 drip A. normalize conduction, automaticity, by acting preferentially on dysfunctional cells (e.g. strong attraction to ischemic tissue or damaged tissue) B. Not effect normal tissue C. Used mainly for VTACH or VFIB (e.g. after MI) Using amiodarone more than Lidocaine D. Side effects (toxicity) too much Lidocaine toxic excitation seizures death apnea disopyramide (Norpace) (Class I-A quinidine-like) A. Used for serious ventricular arrhythmias that dont respond to other drugs B. Intense atropine-like side effects

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Brethylium (Brethylol) Class III A. IV antifibrillatory agent, but not first line, nor for ventricular arrhythmias other than VFIB

Miscellaneous: Adenosine, Digoxin, Atropine, Magnesium Sulfate I. Adenosine (Adenocard) A. Naturally occurring nucleoside B. Acts quickly, has a short half life C. Acts on specific adenosine receptors to increase outward K+ current leading to cell hyperpolarization i. Main effects predominately on AV node to decrease conduction D. IV bolus administration give as close to heart as possible E. Side effect impending doom, chest pain, flushed digoxin (Lanoxin) A. Primarily used to treat heart failure, but also prescribed for certain types of atrial dysrhythmias decrease automaticity of the SA node and slow conduction through the AV node. B. Should be carefully monitored because of excessive levels of digoxin can produce serious dysrhythmias. i. Review Adverse effects Dig toxicity ii. Apical pulse iii. Dig levels (narrow therapeutic window 0.8-2.0 iv. Monitor potassium level (who is more likely to become dig toxic?) C. Used mainly as adjunct to quinidine for initial treatment of supraventricular tachycardias D. Digoxin Immune Fab (Digibind) is antidote of Digitalis toxicity Atropine (parenteral) has ability to block effects of acetylcholine on cardiac (SA nodal) muscarinic receptors, - sinus Bradycardia Magnesium sulfate

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A. Reserved for refractory ventricular arrhythmias, or any arrhythmias, caused by

hypomagnesemia (common in digoxin intoxication, pregnancy, and induced by some diuretics) A = Adenosine B = Beta Blockers C = Calcium Channel Blockers D =Digoxin (long time to take effect) E = Electric conversion